Differential Disturbances of Memory and Mood Following Striatum and Basal Forebrain Lesions in Patients with Ruptures of the Anterior Communicating Artery

For a long time, it has been known that subarachnoid hemorrhage is likely to be followed by Korsakoff’s syndrome [13]. However, in many of the patients, the syndrome is transient. The remaining patients may show persistent anterograde memory deficits, as well as personality changes. This lasting syndrome is often referred to as ACoA (anterior communicating artery) syndrome because it is observed most often following the rupture and repair of an aneurysm of the ACoA [12]. However, the anatomical basis for the syndrome, especially for the memory deficits, is unsettled. Most authors stress the importance of lesions directly related to the territory of the ACoA (i.e., substantia innominata, diagonal band of Broca, ventral striatum); however, in many cases additional lesions were reported to be situated in the frontal cortex, septum, medial forebrain bundle, fornix, anterior hypothalamus, and neostriatum [1,3,4,10]. The present study was undertaken to clarify the lesion loci necessary and sufficient to cause amnesia. We chose our subjects on the basis of their lesions from a population of subjects with subarachnoid hemorrhage, all having undergone treatment and follow-up evaluation at the neurosurgical department of the University of Heidelberg. The subjects were investigated neuropsychologically and compared with subjects with brain tumors in similar loci, and with control subjects without brain damage. The resulting samples were representative and indicated that basal forebrain lesions are necessary to cause amnesia, but are sufficient to cause amnesia only in the presence of additional lesions in the neostriatum.